<?xml version="1.0" encoding="ISO-8859-1"?>

<rdf:RDF
 xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"
 xmlns="http://purl.org/rss/1.0/"
 xmlns:taxo="http://purl.org/rss/1.0/modules/taxonomy/"
 xmlns:dc="http://purl.org/dc/elements/1.1/"
 xmlns:syn="http://purl.org/rss/1.0/modules/syndication/"
 xmlns:prism="http://purl.org/rss/1.0/modules/prism/"
 xmlns:admin="http://webns.net/mvcb/"
>

<channel rdf:about="http://aje.oxfordjournals.org">
<title>American Journal of Epidemiology - Advance Access</title>
<link>http://aje.oxfordjournals.org</link>
<description>American Journal of Epidemiology - RSS feed of articles</description>
<prism:eIssn>1476-6256</prism:eIssn>
<prism:publicationName>American Journal of Epidemiology</prism:publicationName>
<prism:issn>0002-9262</prism:issn>
<items>
 <rdf:Seq>
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp385v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp384v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp311v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp309v2?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp299v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp320v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp308v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp318v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp375v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp374v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp368v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp366v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp348v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp314v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp313v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp297v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp305v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp282v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp321v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp310v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp346v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp307v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp369v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp367v1?rss=1" />
  <rdf:li rdf:resource="http://aje.oxfordjournals.org/cgi/content/short/kwp315v1?rss=1" />
 </rdf:Seq>
</items>
</channel>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp385v1?rss=1">
<title><![CDATA[THE AUTHORS REPLY]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp385v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Stein, C. R., Savitz, D. A.]]></dc:creator>
<dc:date>Wed, 18 Nov 2009 06:17:15 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp385</dc:identifier>
<dc:title><![CDATA[THE AUTHORS REPLY]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-18</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp384v1?rss=1">
<title><![CDATA[RE: "SERUM LEVELS OF PERFLUOROOCTANOIC ACID AND PERFLUOROOCTANE SULFONATE AND PREGNANCY OUTCOME"]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp384v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Fei, C., Olsen, J.]]></dc:creator>
<dc:date>Wed, 18 Nov 2009 06:17:13 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp384</dc:identifier>
<dc:title><![CDATA[RE: "SERUM LEVELS OF PERFLUOROOCTANOIC ACID AND PERFLUOROOCTANE SULFONATE AND PREGNANCY OUTCOME"]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-18</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp311v1?rss=1">
<title><![CDATA[Visceral Fat Volume and the Prevalence of Colorectal Adenoma]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp311v1?rss=1</link>
<description><![CDATA[
<p>Few epidemiologic investigations of visceral adiposity and colorectal neoplasms have attempted the direct quantification of visceral fat. The authors measured visceral fat volume among middle-aged and elderly Japanese men and women who underwent colonoscopy and positron emission tomography/computed tomography for cancer screening in Tokyo, Japan, between February 2004 and February 2005, and examined the association between visceral adiposity and colorectal adenoma in 1,205 eligible subjects. Odds ratios and 95% confidence intervals for colorectal adenoma were estimated by using an unconditional logistic regression model after adjustment for potential confounders. Despite its high correlation with body mass index, visceral fat volume was associated with the prevalence of colorectal adenoma independently of body mass index in both sexes. After further adjustment for body mass index, the odds ratio of colorectal adenoma for the highest compared with the lowest quartile of visceral fat volume was 1.58 (95% confidence interval: 1.11, 2.24) for men and women combined. Conversely, body mass index was unlikely to modify the association between visceral fat volume and colorectal adenoma (<I>P</I><SUB>interaction</SUB> = 0.39). These findings add to accumulating evidence that visceral adiposity exerts an important influence on the pathogenesis of colorectal neoplasms. The mechanisms of this potential association between visceral adiposity and colorectal carcinogenesis warrant further investigation.</p>
]]></description>
<dc:creator><![CDATA[Yamaji, T., Iwasaki, M., Sasazuki, S., Kurahashi, N., Mutoh, M., Yamamoto, S., Suzuki, M., Moriyama, N., Wakabayashi, K., Tsugane, S.]]></dc:creator>
<dc:date>Wed, 18 Nov 2009 06:17:09 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp311</dc:identifier>
<dc:title><![CDATA[Visceral Fat Volume and the Prevalence of Colorectal Adenoma]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-18</prism:publicationDate>
<prism:section>Original Contribution</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp309v2?rss=1">
<title><![CDATA[A Family Longevity Selection Score: Ranking Sibships by Their Longevity, Size, and Availability for Study]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp309v2?rss=1</link>
<description><![CDATA[
<p>Family studies of exceptional longevity can potentially identify genetic and other factors contributing to long life and healthy aging. Although such studies seek families that are exceptionally long lived, they also need living members who can provide DNA and phenotype information. On the basis of these considerations, the authors developed a metric to rank families for selection into a family study of longevity. Their measure, the family longevity selection score (FLoSS), is the sum of 2 components: 1) an estimated family longevity score built from birth-, gender-, and nation-specific cohort survival probabilities and 2) a bonus for older living siblings. The authors examined properties of FLoSS-based family rankings by using data from 3 ongoing studies: the New England Centenarian Study, the Framingham Heart Study, and screenees for the Long Life Family Study. FLoSS-based selection yields families with exceptional longevity, satisfactory sibship sizes and numbers of living siblings, and high ages. Parameters in the FLoSS formula can be tailored for studies of specific populations or age ranges or with different conditions. The first component of the FLoSS also provides a conceptually sound survival measure to characterize exceptional longevity in individuals or families in various types of studies and correlates well with later-observed longevity.</p>
]]></description>
<dc:creator><![CDATA[Sebastiani, P., Hadley, E. C., Province, M., Christensen, K., Rossi, W., Perls, T. T., Ash, A. S.]]></dc:creator>
<dc:date>Wed, 18 Nov 2009 06:16:58 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp309</dc:identifier>
<dc:title><![CDATA[A Family Longevity Selection Score: Ranking Sibships by Their Longevity, Size, and Availability for Study]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-18</prism:publicationDate>
<prism:section>Practice of Epidemiology</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp299v1?rss=1">
<title><![CDATA[Validity of Adolescent Diet Recall 48 Years Later]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp299v1?rss=1</link>
<description><![CDATA[
<p>Few studies have evaluated the validity of adolescent diet recall after many decades. Between 1943 and 1970, yearly diet records were completed by parents of adolescents participating in an ongoing US study. In 2005&ndash;2006, study participants who had been 13&ndash;18 years of age when the diet records were collected were asked to complete a food frequency questionnaire regarding their adolescent diet. Food frequency questionnaires and diet records were available for 72 participants. The authors calculated Spearman correlation coefficients between food, food group, and nutrient intakes from the diet records and food frequency questionnaire and deattenuated them to account for the effects of within-person variation measured in the diet records on the association. The median deattenuated correlation for foods was 0.30, ranging from &ndash;0.53 for a beef, pork, or lamb sandwich to 0.99 for diet soda. The median deattenuated correlation for food groups was 0.31 (range: &ndash;0.48 for breads to 0.70 for hot beverages); for nutrient intakes, it was 0.25 (range: &ndash;0.08 for iron to 0.82 for vitamin B<SUB>12</SUB>). Some dietary factors were reasonably recalled 3&ndash;6 decades later. However, this food frequency questionnaire did not validly measure overall adolescent diet when completed by middle-aged and older adults on average 48 years after adolescence.</p>
]]></description>
<dc:creator><![CDATA[Chavarro, J. E., Rosner, B. A., Sampson, L., Willey, C., Tocco, P., Willett, W. C., Chumlea, Wm. C., Michels, K. B.]]></dc:creator>
<dc:date>Wed, 18 Nov 2009 06:16:52 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp299</dc:identifier>
<dc:title><![CDATA[Validity of Adolescent Diet Recall 48 Years Later]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-18</prism:publicationDate>
<prism:section>Practice of Epidemiology</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp320v1?rss=1">
<title><![CDATA[Low-Grade, Systemic Inflammation in Adolescents: Association With Early-Life Factors, Gender, and Lifestyle]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp320v1?rss=1</link>
<description><![CDATA[
<p>Low-grade, systemic inflammation is related to increased risk of cardiovascular disease in adults. The proinflammatory state tracks from adolescence to adulthood. Identifying correlates of inflammation in adolescents could provide opportunities to prevent cardiovascular disease in adulthood. However, population-based data on correlates of inflammation in adolescence are limited. Therefore, the authors studied the associations of early-life factors, gender, and lifestyle with inflammation (measured by high-sensitivity C-reactive protein and leukocyte count) at age 16 years (2001&ndash;2002) in the prospective, population-based Northern Finland Birth Cohort 1986 Study (<I>n</I> = 5,240). In females, being born small for gestational age and current use of oral contraceptives were associated with the proinflammatory state. The association of birth size with inflammation was not observed in males. In logistic regression analyses, oral contraceptive use (odds ratio (OR) = 2.83), abdominal obesity (OR = 5.17), and smoking (OR = 2.72) were associated with elevation of both inflammation markers in females; abdominal obesity (OR = 5.72) and smoking (OR = 2.02) were associated in males. Thus, females appear more susceptible to the adverse effects of being born small for gestational age than males. Given the widespread use of oral contraceptives and the potential pathophysiologic consequences of the proinflammatory state, the association of oral contraceptive use with inflammation in adolescence may have public health implications.</p>
]]></description>
<dc:creator><![CDATA[Pirkola, J., Vaarasmaki, M., Ala-Korpela, M., Bloigu, A., Canoy, D., Hartikainen, A.-L., Leinonen, M., Miettola, S., Paldanius, M., Tammelin, T. H., Jarvelin, M.-R., Pouta, A.]]></dc:creator>
<dc:date>Mon, 16 Nov 2009 02:46:43 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp320</dc:identifier>
<dc:title><![CDATA[Low-Grade, Systemic Inflammation in Adolescents: Association With Early-Life Factors, Gender, and Lifestyle]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-16</prism:publicationDate>
<prism:section>Original Contribution</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp308v1?rss=1">
<title><![CDATA[Smoking and Risk of Tuberculosis Incidence, Mortality, and Recurrence in South Korean Men and Women]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp308v1?rss=1</link>
<description><![CDATA[
<p>The authors explored the association of cigarette smoking with tuberculosis incidence, recurrence, and mortality. A 14-year prospective cohort study (1992&ndash;2006) was carried out in 1,294,504 South Koreans. Participants were grouped by smoking history, and the authors assessed tuberculosis incidence, mortality, and recurrence risk for each group. Unadjusted and adjusted Cox proportional hazards models were used to investigate the association between smoking history and the 3 outcomes of interest, adjusting for age and alcohol use. Compared with never smokers, current smokers had increased mortality from tuberculosis among both men (adjusted hazard ratio (HR) = 1.6, 95% confidence interval (CI): 1.3, 2.0) and women (HR = 1.6, 95% CI: 1.0, 2.4). Current male smokers had greater risk of incident tuberculosis than former smokers (HR = 1.4, 95% CI: 1.3, 1.5), and risk among current smokers increased with number of cigarettes smoked daily. In females, cigarette smoking was not associated with incident tuberculosis. There was interaction between smoking and sex for incidence (<I>P</I> = 0.00047). The effect of smoking was generally reduced with adjustment for body mass index. Among men, the highest alcohol consumption category (&ge;100 g/day) was associated with risk of incident tuberculosis (HR = 1.5, 95% CI: 1.3, 1.7). This study provides longitudinal evidence that smoking increases risk of incident tuberculosis, mortality from tuberculosis, and tuberculosis recurrence.</p>
]]></description>
<dc:creator><![CDATA[Jee, S. H., Golub, J. E., Jo, J., Park, I. S., Ohrr, H., Samet, J. M.]]></dc:creator>
<dc:date>Mon, 16 Nov 2009 02:46:39 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp308</dc:identifier>
<dc:title><![CDATA[Smoking and Risk of Tuberculosis Incidence, Mortality, and Recurrence in South Korean Men and Women]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-16</prism:publicationDate>
<prism:section>Original Contribution</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp318v1?rss=1">
<title><![CDATA[Steroid 5-{alpha}-Reductase Type 2 (SRD5a2) Gene Polymorphisms and Risk of Prostate Cancer: A HuGE Review]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp318v1?rss=1</link>
<description><![CDATA[
<p>Steroid 5--reductase type 2 (SRD5a2) is a critical enzyme in androgen metabolism. Two polymorphisms in the <I>SRD5a2</I> gene, <I>V89L</I> (rs523349) and <I>A49T</I> (rs9282858), have been studied for associations with prostate cancer risk, with conflicting results. The authors conducted a systematic review and meta-analysis (1997&ndash;2007) to examine these associations and compared the results with findings from genome-wide association studies of prostate cancer. The meta-analysis included 24 case-control studies (10,088 cases and 10,120 controls for <I>V89L</I> and 4,998 cases and 5,451 controls for <I>A49T</I>). The authors found that prostate cancer was not associated with <I>V89L</I> (<I>L</I> allele vs. <I>V</I> allele: odds ratio = 0.99, 95% confidence interval: 0.94, 1.05) and was probably not associated with <I>A49T</I> (<I>T</I> allele vs. <I>A</I> allele: odds ratio = 1.10, 95% confidence interval: 0.86, 1.40). These results could have been distorted by spectrum-of-disease bias, convenience sampling of cases and controls, genotype misclassification, and/or confounding. Neither <I>V89L</I> nor <I>A49T</I> was included in microarray chips used for published genome-wide association studies. Analysis of well-designed population-based studies with pathway-based arrays containing common genetic variants could be useful for identifying genetic factors in prostate cancer.</p>
]]></description>
<dc:creator><![CDATA[Li, J., Coates, R. J., Gwinn, M., Khoury, M. J.]]></dc:creator>
<dc:date>Fri, 13 Nov 2009 04:23:53 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp318</dc:identifier>
<dc:title><![CDATA[Steroid 5-{alpha}-Reductase Type 2 (SRD5a2) Gene Polymorphisms and Risk of Prostate Cancer: A HuGE Review]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-13</prism:publicationDate>
<prism:section>Human Genome Epidemiology (HuGE) Review</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp375v1?rss=1">
<title><![CDATA[Molecular Sequence Data of Hepatitis B Virus and Genetic Diversity After Vaccination]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp375v1?rss=1</link>
<description><![CDATA[
<p>The effect of vaccination programs on transmission of infectious disease is usually assessed by monitoring programs that rely on notifications of symptomatic illness. For monitoring of infectious diseases with a high proportion of asymptomatic cases or a low reporting rate, molecular sequence data combined with modern coalescent-based techniques offer a complementary tool to assess transmission. Here, the authors investigate the added value of using viral sequence data to monitor a vaccination program that was started in 1998 and was targeted against hepatitis B virus in men who have sex with men in Amsterdam, the Netherlands. The incidence in this target group, as estimated from the notifications of acute infections with hepatitis B virus, was low; therefore, there was insufficient power to show a significant change in incidence. In contrast, the genetic diversity, as estimated from the viral sequence collected from the target group, revealed a marked decrease after vaccination was introduced. Taken together, the findings suggest that introduction of vaccination coincided with a change in the target group toward behavior with a higher risk of infection. The authors argue that molecular sequence data provide a powerful additional monitoring instrument, next to conventional case registration, for assessing the impact of vaccination.</p>
]]></description>
<dc:creator><![CDATA[van Ballegooijen, W. M., van Houdt, R., Bruisten, S. M., Boot, H. J., Coutinho, R. A., Wallinga, J.]]></dc:creator>
<dc:date>Thu, 12 Nov 2009 01:40:56 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp375</dc:identifier>
<dc:title><![CDATA[Molecular Sequence Data of Hepatitis B Virus and Genetic Diversity After Vaccination]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-12</prism:publicationDate>
<prism:section>Original Contribution</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp374v1?rss=1">
<title><![CDATA[Eras in Epidemiology: The Evolution of Ideas: By Mervyn Susser and Zena Stein]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp374v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Morabia, A.]]></dc:creator>
<dc:date>Thu, 12 Nov 2009 01:40:54 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp374</dc:identifier>
<dc:title><![CDATA[Eras in Epidemiology: The Evolution of Ideas: By Mervyn Susser and Zena Stein]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-12</prism:publicationDate>
<prism:section>Book Review</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp368v1?rss=1">
<title><![CDATA[Van Ballegooijen et al. Respond to "Evaluating Vaccination Programs Using Genetic Sequence Data"]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp368v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[van Ballegooijen, W. M., van Houdt, R., Bruisten, S. M., Boot, H. J., Coutinho, R. A., Wallinga, J.]]></dc:creator>
<dc:date>Thu, 12 Nov 2009 01:40:53 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp368</dc:identifier>
<dc:title><![CDATA[Van Ballegooijen et al. Respond to "Evaluating Vaccination Programs Using Genetic Sequence Data"]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-12</prism:publicationDate>
<prism:section>Response to Invited Commentary</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp366v1?rss=1">
<title><![CDATA[Invited Commentary: Evaluating Vaccination Programs Using Genetic Sequence Data]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp366v1?rss=1</link>
<description><![CDATA[
<p>Genomic data will become an increasingly important component of epidemiologic studies in coming years. The authors of the accompanying <I>Journal</I> article, van Ballegooijen et al. (<I>Am J Epidemiol</I>. <b>2009;XXX(XX):000&ndash;000</b>), are to be commended for attempting to use the coalescent analysis of viral sequence data to evaluate a hepatitis B vaccination program. Coalescent theory attempts to link the phylogenetic history of populations with rates of population growth and decline. In particular, under certain assumptions, a reduction in genetic diversity can be interpreted as a reduction in disease incidence. However, the authors of this commentary contend that van Ballegooijen et al.&rsquo;s interpretation of changes in viral genetic diversity as a measure of hepatitis B vaccine effectiveness has major limitations. Because of the potential use of these methods in future vaccination studies, the authors discuss the utility of these methods and the data requirements needed for them to be convincing. First, data sets should be large enough to provide sufficient epidemiologic-scale resolution. Second, data need to reflect sufficiently fine-grained temporal sampling. Third, other processes that can potentially influence genetic diversity and confuse demographic inferences should be considered.</p>
]]></description>
<dc:creator><![CDATA[Halloran, M. E., Holmes, E. C.]]></dc:creator>
<dc:date>Thu, 12 Nov 2009 01:40:52 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp366</dc:identifier>
<dc:title><![CDATA[Invited Commentary: Evaluating Vaccination Programs Using Genetic Sequence Data]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-12</prism:publicationDate>
<prism:section>Invited Commentary</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp348v1?rss=1">
<title><![CDATA[Re: "Associations of Gestational Weight Gain With Short- and Longer-Term Maternal and Child Health Outcomes"]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp348v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Ruiz, J. R., Barakat, R., Lucia, A.]]></dc:creator>
<dc:date>Thu, 12 Nov 2009 01:40:51 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp348</dc:identifier>
<dc:title><![CDATA[Re: "Associations of Gestational Weight Gain With Short- and Longer-Term Maternal and Child Health Outcomes"]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-12</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp314v1?rss=1">
<title><![CDATA[Risk Factors for Epithelial Ovarian Cancer by Histologic Subtype]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp314v1?rss=1</link>
<description><![CDATA[
<p>Previous epidemiologic studies suggest that the major histologic subtypes of epithelial ovarian cancer may have different risk factor profiles; however, no known prospective study has systematically examined differences in risk by subtype. The authors used Cox proportional hazards regression, stratified by histologic subtype and time period, to examine the association between ovarian cancer risk factors and incidence of serous invasive, endometrioid, and mucinous ovarian cancers in the US Nurses&rsquo; Health Study (1976&ndash;2006) and Nurses&rsquo; Health Study II (1989&ndash;2005). For each exposure, they calculated <I>P</I>-heterogeneity using a likelihood ratio test comparing models with separate estimates for the 3 subtypes versus a single estimate across subtypes. Analysis included 221,866 women and 721 cases with the histologies of interest (496 serous invasive, 139 endometrioid, 86 mucinous). In analyses of reproductive/hormonal exposures, the associations with age, duration of breastfeeding, age at natural menopause, and duration of estrogen use differed significantly by subtype (all <I>P</I>-heterogeneity &le;0.05). The associations with several nonreproductive exposures also appeared to vary by subtype, but only the association with smoking differed significantly (<I>P</I>-heterogeneity = 0.03). Results suggest that associations with several ovarian cancer risk factors vary by subtype, and these differences are consistent with known similarities between each major histologic subtype and its normal tissue counterpart.</p>
]]></description>
<dc:creator><![CDATA[Gates, M. A., Rosner, B. A., Hecht, J. L., Tworoger, S. S.]]></dc:creator>
<dc:date>Thu, 12 Nov 2009 01:40:51 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp314</dc:identifier>
<dc:title><![CDATA[Risk Factors for Epithelial Ovarian Cancer by Histologic Subtype]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-12</prism:publicationDate>
<prism:section>Original Contribution</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp313v1?rss=1">
<title><![CDATA[Determinants of Percentage and Area Measures of Mammographic Density]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp313v1?rss=1</link>
<description><![CDATA[
<p>Mammographic density is one of the strongest predictors of breast cancer risk. Typically expressed as a percentage of the breast area occupied by radiologically dense tissue on a mammogram, its full value may not be realized because of its negative association with body mass index. A simpler measure of mammographic density, independent of other breast cancer risk factors and equally predictive of risk, would be preferable for risk prediction models. Percentage and area measures of mammographic density were determined for 815 women at high risk for breast cancer from the baseline assessments in the International Breast Cancer Intervention Study I, a trial of tamoxifen for breast cancer prevention conducted between 1992 and 2001. Multivariate linear regression was used to assess associations between risk factors and the mammographic measures. Percent dense area was negatively associated with age, body mass index, menopausal status, predicted risk, and smoking status (<I>R</I><sup>2</sup> = 24%). Dense area was negatively associated with only age and body mass index (<I>R</I><sup>2</sup> = 7%), and the latter association was much weaker than for percent dense area. Nondense area was positively associated with age, body mass index, and predicted risk (<I>R</I><sup>2</sup> = 36%). Dense area was not associated with the multitude of risk factors that percent dense area was, making it a simpler biomarker for risk prediction modeling. Both dense area and percent dense area should be presented whenever possible for comparisons in research.</p>
]]></description>
<dc:creator><![CDATA[Stone, J., Warren, R. M. L., Pinney, E., Warwick, J., Cuzick, J.]]></dc:creator>
<dc:date>Thu, 12 Nov 2009 01:40:49 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp313</dc:identifier>
<dc:title><![CDATA[Determinants of Percentage and Area Measures of Mammographic Density]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-12</prism:publicationDate>
<prism:section>Practice of Epidemiology</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp297v1?rss=1">
<title><![CDATA[Sporadic Gastroenteritis and Recreational Swimming in a Longitudinal Community Cohort Study in Melbourne, Australia]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp297v1?rss=1</link>
<description><![CDATA[
<p>The relation between sporadic gastroenteritis and recreational swimming was examined in a cohort of 2,811 people in Melbourne, Australia, over a 15-month period (September 1997&ndash;February 1999). Data from a prospective community-based study of gastroenteritis were used for a Poisson analysis of temporality between reported swimming (in public or private pools/spas and in marine or freshwater settings) and a highly credible gastroenteritis (HCG) event. Overall, HCG events were more likely in participants who had swum in a public pool/spa (incidence rate ratio (IRR) = 1.25, 95% confidence interval (CI): 1.10, 1.42; <I>P</I> = 0.001) or river/lake/dam (IRR = 1.77, 95% CI: 1.13, 2.79; <I>P</I> = 0.014) during the previous week or had swum in a public pool/spa (IRR = 1.29, 95% CI: 1.13, 1.46; <I>P</I> &lt; 0.001) during the previous 2 weeks. Subanalysis by age showed that HCG episodes were also more likely in adults who had swum in a private pool/spa (IRR = 1.56, 95% CI: 1.02, 2.39; <I>P</I> = 0.042) during the previous week or swum at an ocean/beach (IRR = 1.78, 95% CI: 1.12, 2.81; <I>P</I> = 0.014) during the previous 2 weeks, demonstrating significant associations between all swimming locations and gastrointestinal symptoms. This study showed that although the incremental risk of recreational swimming is significant, it is relatively small.</p>
]]></description>
<dc:creator><![CDATA[Dale, K., Wolfe, R., Sinclair, M., Hellard, M., Leder, K.]]></dc:creator>
<dc:date>Wed, 11 Nov 2009 03:38:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp297</dc:identifier>
<dc:title><![CDATA[Sporadic Gastroenteritis and Recreational Swimming in a Longitudinal Community Cohort Study in Melbourne, Australia]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-11</prism:publicationDate>
<prism:section>Original Contribution</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp305v1?rss=1">
<title><![CDATA[Importance of Routine Public Health Influenza Surveillance: Detection of an Unusual W-Shaped Influenza Morbidity Curve]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp305v1?rss=1</link>
<description><![CDATA[
<p>Seasonal influenza causes excess morbidity and mortality at the extremes of age: It disproportionately affects the very young and the very old, typically resulting in "U"-shaped age-distributed curves. By means of a well-established public health department surveillance system using positive influenza tests submitted from sentinel sites, the authors generated annual influenza-specific morbidity curves over a 10-year period (1998&ndash;2008) for St. Louis County, Missouri. The authors detected an unusually high incidence of cases of medically attended test-positive influenza, particularly in young adults, during the 2007&ndash;2008 season, resulting in an unexpected "W"-shaped age-distributed morbidity curve that was distinctly unique in comparison with the prior 9 influenza seasons. Public health influenza surveillance programs are useful tools for detecting emerging epidemiologic trends that may have clinical importance.</p>
]]></description>
<dc:creator><![CDATA[Georgantopoulos, P., Bergquist, E. P., Knaup, R. C., Anthony, J. R., Bailey, T. C., Williams, M. P., Lawrence, S. J.]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 04:53:17 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp305</dc:identifier>
<dc:title><![CDATA[Importance of Routine Public Health Influenza Surveillance: Detection of an Unusual W-Shaped Influenza Morbidity Curve]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-10</prism:publicationDate>
<prism:section>Practice of Epidemiology</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp282v1?rss=1">
<title><![CDATA[Adherence to the Mediterranean Diet and Risk of Coronary Heart Disease in the Spanish EPIC Cohort Study]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp282v1?rss=1</link>
<description><![CDATA[
<p>No known cohort study has investigated whether the Mediterranean diet can reduce incident coronary heart disease (CHD) events in a Mediterranean population. This study examined the relation between Mediterranean diet adherence and risk of incident CHD events in the 5 Spanish centers of the European Prospective Investigation into Cancer and Nutrition. Analysis included 41,078 participants aged 29&ndash;69 years, recruited in 1992&ndash;1996 and followed up until December 2004 (mean follow-up:10.4 years). Confirmed incident fatal and nonfatal CHD events were analyzed according to Mediterranean diet adherence, measured by using an 18-unit relative Mediterranean diet score. A total of 609 participants (79% male) had a fatal or nonfatal confirmed acute myocardial infarction (<I>n</I> = 468) or unstable angina requiring revascularization (<I>n</I> = 141). After stratification by center and age and adjustment for recognized CHD risk factors, high compared with low relative Mediterranean diet score was associated with a significant reduction in CHD risk (hazard ratio = 0.60, 95% confidence interval: 0.47, 0.77). A 1-unit increase in relative Mediterranean diet score was associated with a 6% reduced risk of CHD (95% confidence interval: 0.91, 0.97), with similar risk reductions by sex. Mediterranean diet adherence was associated with a significantly reduced CHD risk in this Mediterranean country, supporting its role in primary prevention of CHD in healthy populations.</p>
]]></description>
<dc:creator><![CDATA[Buckland, G., Gonzalez, C. A., Agudo, A., Vilardell, M., Berenguer, A., Amiano, P., Ardanaz, E., Arriola, L., Barricarte, A., Basterretxea, M., Chirlaque, M. D., Cirera, L., Dorronsoro, M., Egues, N., Huerta, J. M., Larranaga, N., Marin, P., Martinez, C., Molina, E., Navarro, C., Quiros, J. R., Rodriguez, L., Sanchez, M.-J., Tormo, M.-J., Moreno-Iribas, C.]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 04:53:15 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp282</dc:identifier>
<dc:title><![CDATA[Adherence to the Mediterranean Diet and Risk of Coronary Heart Disease in the Spanish EPIC Cohort Study]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-10</prism:publicationDate>
<prism:section>Original Contribution</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp321v1?rss=1">
<title><![CDATA[Use of Nonsteroidal Antiinflammatory Drugs and Risk of Endometrial Cancer]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp321v1?rss=1</link>
<description><![CDATA[
<p>Results of 3 previous studies suggest that use of aspirin is related to a reduced risk of endometrial cancer, at least in obese women (body mass index, &ge;30 kg/m<sup>2</sup>). Using data obtained in a population-based, case-control study in western Washington State, the authors examined this question. Between 2003 and 2005, 410 women diagnosed with invasive endometrial cancer and 356 controls were interviewed regarding the use of aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs). A history of use of NSAIDs was not associated with the risk of endometrial cancer (odds ratio = 1.04, 95% confidence interval: 0.76, 1.42). The lack of association was also present specifically for use of aspirin (odds ratio = 1.06, 95% confidence interval: 0.73, 1.53). NSAID use was unrelated to risk of endometrial cancer in both obese and nonobese women. Results from this study suggest that the use of aspirin or other NSAIDs has little or no influence on the risk of endometrial cancer.</p>
]]></description>
<dc:creator><![CDATA[Bodelon, C., Doherty, J. A., Chen, C., Rossing, M. A., Weiss, N. S.]]></dc:creator>
<dc:date>Fri, 06 Nov 2009 01:08:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp321</dc:identifier>
<dc:title><![CDATA[Use of Nonsteroidal Antiinflammatory Drugs and Risk of Endometrial Cancer]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-06</prism:publicationDate>
<prism:section>Original Contribution</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp310v1?rss=1">
<title><![CDATA[Functional Variants in the Catalase and Myeloperoxidase Genes, Ambient Air Pollution, and Respiratory-related School Absences: An Example of Epistasis in Gene-Environment Interactions]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp310v1?rss=1</link>
<description><![CDATA[
<p>The individual effect of functional single nucleotide polymorphisms within the catalase and myeloperoxidase genes (<I>CAT</I> and <I>MPO</I>) has been studied in relation to asthma; however, their interrelationship with ambient air pollution exposures has yet to be determined. The authors investigated the interrelationships between variants in <I>CAT</I> and <I>MPO</I>, ambient air pollutants, and acute respiratory illness. Health information, air pollution, and incident respiratory-related school absences were ascertained in January&ndash;June 1996 for 1,136 Hispanic and non-Hispanic white US elementary schoolchildren as part of the prospective Children's Health Study. Functional and tagging single nucleotide polymorphisms for the <I>CAT</I> and <I>MPO</I> loci were genotyped. The authors found epistasis between functional polymorphisms in the <I>CAT/MPO</I> loci, which differed by levels of oxidant-stress-producing air pollutants. Risk of respiratory-related school absences was elevated for children with the <I>CAT</I> (G/G) and <I>MPO</I> (G/A or A/A) genes (relative risk = 1.35, 95% confidence interval: 1.03, 1.77; <I>P</I>-interaction = 0.005). The epistatic effect of <I>CAT</I> and <I>MPO</I> variants was most evident in communities exhibiting high ambient ozone levels (<I>P</I>-interaction = 0.03). The association of respiratory-illness absences with functional variants in <I>CAT</I> and <I>MPO</I> that differ by air pollution levels illustrates the need to consider genetic epistasis in assessing gene-environment interactions.</p>
]]></description>
<dc:creator><![CDATA[Wenten, M., Gauderman, W. J., Berhane, K., Lin, P.-C., Peters, J., Gilliland, F. D.]]></dc:creator>
<dc:date>Fri, 06 Nov 2009 01:08:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp310</dc:identifier>
<dc:title><![CDATA[Functional Variants in the Catalase and Myeloperoxidase Genes, Ambient Air Pollution, and Respiratory-related School Absences: An Example of Epistasis in Gene-Environment Interactions]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-06</prism:publicationDate>
<prism:section>Original Contribution</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp346v1?rss=1">
<title><![CDATA[Harold A. Kahn (1920-2009): A Remembrance of a Life Devoted to Public Health]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp346v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Sempos, C. T., Goldbourt, U.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 01:40:18 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp346</dc:identifier>
<dc:title><![CDATA[Harold A. Kahn (1920-2009): A Remembrance of a Life Devoted to Public Health]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-03</prism:publicationDate>
<prism:section>Obituary</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp307v1?rss=1">
<title><![CDATA[Population-based, Case-Control-Family Design to Investigate Genetic and Environmental Influences on Melanoma Risk: Australian Melanoma Family Study]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp307v1?rss=1</link>
<description><![CDATA[
<p>Discovering and understanding genetic risk factors for melanoma and their interactions with phenotype, sun exposure, and other risk factors could lead to new strategies for melanoma control. This paper describes the Australian Melanoma Family Study, which uses a multicenter, population-based, case-control-family design. From 2001 to 2005, the authors recruited 1,164 probands including 629 cases with histopathologically confirmed, first-primary cutaneous melanoma diagnosed before age 40 years, 240 population-based controls frequency matched for age, and 295 spouse/friend controls. Information on lifetime sun exposure, phenotype, and residence history was collected for probands and nearly 4,000 living relatives. More than 3,000 subjects donated a blood sample. Proxy-reported information was collected for childhood sun exposure and deceased relatives. Important features of this study include the population-based, family-based design; a focus on early onset disease; probands from 3 major cities differing substantially in solar ultraviolet exposure and melanoma incidence; a population at high risk because of high ultraviolet exposure and susceptible pigmentation phenotypes; population-based, spouse/friend, and sibling controls; systematic recruitment of relatives of case and control probands; self and parent reports of childhood sun exposure; and objective clinical skin examinations. The authors discuss methodological and analytical issues related to the study design and conduct, as well as the potentially novel insights the study can deliver.</p>
]]></description>
<dc:creator><![CDATA[Cust, A. E., Schmid, H., Maskiell, J. A., Jetann, J., Ferguson, M., Holland, E. A., Agha-Hamilton, C., Jenkins, M. A., Kelly, J., Kefford, R. F., Giles, G. G., Armstrong, B. K., Aitken, J. F., Hopper, J. L., Mann, G. J.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 01:40:17 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp307</dc:identifier>
<dc:title><![CDATA[Population-based, Case-Control-Family Design to Investigate Genetic and Environmental Influences on Melanoma Risk: Australian Melanoma Family Study]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-03</prism:publicationDate>
<prism:section>Practice of Epidemiology</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp369v1?rss=1">
<title><![CDATA[THE FIRST AUTHOR REPLIES]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp369v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Salomon, J. A.]]></dc:creator>
<dc:date>Sun, 01 Nov 2009 23:23:45 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp369</dc:identifier>
<dc:title><![CDATA[THE FIRST AUTHOR REPLIES]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp367v1?rss=1">
<title><![CDATA[RE: "ARE AMERICANS FEELING LESS HEALTHY? THE PUZZLE OF TRENDS IN SELF-RATED HEALTH"]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp367v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Avendano, M., Huijts, T., Subramanian, S. V.]]></dc:creator>
<dc:date>Sun, 01 Nov 2009 23:23:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp367</dc:identifier>
<dc:title><![CDATA[RE: "ARE AMERICANS FEELING LESS HEALTHY? THE PUZZLE OF TRENDS IN SELF-RATED HEALTH"]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://aje.oxfordjournals.org/cgi/content/short/kwp315v1?rss=1">
<title><![CDATA[Effect of Supplemental Folic Acid in Pregnancy on Childhood Asthma: A Prospective Birth Cohort Study]]></title>
<link>http://aje.oxfordjournals.org/cgi/content/short/kwp315v1?rss=1</link>
<description><![CDATA[
<p>This study aimed to investigate the effect of the timing, dose, and source of folate during pregnancy on childhood asthma by using data from an Australian prospective birth cohort study (<I>n</I> = 557) from 1998 to 2005. At 3.5 years and 5.5 years, 490 and 423 mothers and children participated in the study, respectively. Maternal folate intake from diet and supplements was assessed by food frequency questionnaire in early (&lt;16 weeks) and late (30&ndash;34 weeks) pregnancy. The primary outcome was physician-diagnosed asthma, obtained by maternal-completed questionnaire. Asthma was reported in 11.6% of children at 3.5 years (<I>n</I> = 57) and in 11.8% of children at 5.5 years (<I>n</I> = 50). Folic acid taken in supplement form in late pregnancy was associated with an increased risk of childhood asthma at 3.5 years (relative risk (RR) = 1.26, 95% confidence interval (CI): 1.08, 1.43) and with persistent asthma (RR = 1.32, 95% CI: 1.03, 1.69). The effect sizes did not change with adjustment for potential confounders. The association was similar at 5.5 years but did not reach statistical significance (RR = 1.17, 95% CI: 0.96, 1.42) in univariable models. These findings on childhood asthma support previous observations that supplementation with folate in pregnancy leads to an allergic asthma phenotype in mice via epigenetic mechanisms and is associated with poorer respiratory outcomes in young children.</p>
]]></description>
<dc:creator><![CDATA[Whitrow, M. J., Moore, V. M., Rumbold, A. R., Davies, M. J.]]></dc:creator>
<dc:date>Fri, 30 Oct 2009 07:03:41 PDT</dc:date>
<dc:identifier>info:doi/10.1093/aje/kwp315</dc:identifier>
<dc:title><![CDATA[Effect of Supplemental Folic Acid in Pregnancy on Childhood Asthma: A Prospective Birth Cohort Study]]></dc:title>
<dc:publisher>Oxford University Press</dc:publisher>
<prism:publicationDate>2009-10-30</prism:publicationDate>
<prism:section>Original Contribution</prism:section>
</item>

</rdf:RDF>